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1 rognostic factor associated with progressive lymphocytosis.
2 eristic lymphocyte clone and the presence of lymphocytosis.
3 mal blood count and 13.9% (309 of 2228) with lymphocytosis.
4 50% of cases of CD4(+) T-cell large granular lymphocytosis.
5 microl), with 56% of patients experiencing a lymphocytosis.
6 ammation, often granulomatous, and meningeal lymphocytosis.
7 vels with only a few cases developing marked lymphocytosis.
8 okine production by T cells and induction of lymphocytosis.
9 an indolent lymphoma with monoclonal B-cell lymphocytosis.
10 (-/-) mice failed to develop splenomegaly or lymphocytosis.
11 velopment and/or maintenance of persistent B lymphocytosis.
12 e with the preneoplastic syndrome persistent lymphocytosis.
13 phadenopathy or significant peripheral blood lymphocytosis.
14 a significant decrease of monoclonal B-cell lymphocytosis.
15 1 IWCLL partial response (PR) and 3 PRs with lymphocytosis.
16 onse criteria modified for treatment-related lymphocytosis.
17 ymerase chain reaction and leukocytosis with lymphocytosis.
18 68%; 38 (34%) of 111 patients had transient lymphocytosis.
19 who achieved nodal response with persistent lymphocytosis.
20 on samples from nine patients with prolonged lymphocytosis.
21 sulted in the near abolishment of the B cell lymphocytosis.
22 treated patients had a partial response with lymphocytosis.
23 espective groups had a partial response with lymphocytosis.
24 ed by a more benign monoclonal CD5(+) B-cell lymphocytosis.
25 taken into account when considering duodenal lymphocytosis.
26 que family with hereditary polyclonal B cell lymphocytosis.
27 e the CLL precursor lesion monoclonal B cell lymphocytosis.
28 than 50% in 19 of 21 patients with baseline lymphocytosis.
29 romote cell proliferation and does not cause lymphocytosis.
30 g rapid lymph node shrinkage and a transient lymphocytosis.
31 n the preleukemic state of monoclonal B-cell lymphocytosis.
32 RC3 lesions were absent in monoclonal B-cell lymphocytosis (0 of 63) and were rare in CLL at diagnosi
33 pdated criteria of PR with treatment-induced lymphocytosis.(1,2) The median progression-free survival
34 hemotherapy, 13 patients with large granular lymphocytosis, 20 controls who had received renal allogr
36 leucocytosis (64 versus 22%, P: < 0.05), CSF lymphocytosis (64 versus 42%, not significant) and CSF p
37 is (frequency 99.9%, 95% CI 68.5-100.0), CSF lymphocytosis (97.9%, 51.9-100.0), fever (89.8%, 79.8-95
39 f IL-2 administered, and the maximal rebound lymphocytosis after cessation of IL-2 correlated with ac
40 ons after DLI developed a significant B-cell lymphocytosis after treatment, which did not occur in pa
42 had raised CSF protein levels and 73% had a lymphocytosis, although 57% of all submitted samples sho
46 D and correlate with the degree of pulmonary lymphocytosis and clinical measures of disease severity.
48 characterized by chronic cerebrospinal fluid lymphocytosis and elevated levels of the antiviral cytok
51 , the authors discuss the current work-up of lymphocytosis and highlight how to use recently identifi
52 h upon repeated TCR engagement and pulmonary lymphocytosis and hyperinflammation in Mtb-infected mice
53 ) patients with CD4(+) T-cell large granular lymphocytosis and implicate cytomegalovirus as a likely
54 le of cytomegalovirus (CMV) infection in CD8 lymphocytosis and inflammation in ART-treated HIV infect
55 y of patients, even before the occurrence of lymphocytosis and irrespective of the clonotypic IGH var
56 OR1 x TCL1) developed CD5(+)B220(low) B-cell lymphocytosis and leukemia at a significantly younger me
60 account for a significant proportion of the lymphocytosis and provide molecular evidence that these
61 rently healthy Ppp1r18-/- mice that manifest lymphocytosis and reduced population of peripheral lymph
62 cells' survival during BTK inhibitor-induced lymphocytosis and/or playing a role in therapy resistanc
63 itive group, 17 animals exhibited persistent lymphocytosis, and 100% of these were herpesvirus positi
64 mice deficient in IL-2 exhibit splenomegaly, lymphocytosis, and autoimmunity, suggesting this cytokin
66 d serial samples during ibrutinib-associated lymphocytosis, and identified clades of cells that were
67 of antigen exposure, bronchoalveolar lavage lymphocytosis, and lung biopsy demonstrating granulomas,
68 nd that medullary carcinoma, intraepithelial lymphocytosis, and poor differentiation were the best di
69 is model, PCI-32765 caused a transient early lymphocytosis, and profoundly inhibited CLL progression,
70 staining included marked tumor infiltrating lymphocytosis, and solid/cribiform or signet ring histol
71 receiving ibrutinib who have residual clonal lymphocytosis, and that clinical trials are needed to ev
72 hypergammaglobulinemia, autoimmunity, B-cell lymphocytosis, and the expansion of an unusual populatio
73 ures are associated with cerebrospinal fluid lymphocytosis, and the later features with appearance of
74 expand, suggesting that the profound CD8(+) lymphocytosis associated with acute EBV infection is com
76 evelop an early-onset indolent CD5(+) B-cell lymphocytosis attributed to a defect in secondary V(D)J
77 e shrinkage, along with a transient surge in lymphocytosis, before inducing objective remissions.
79 or complement factors C1q, monoclonal B-cell lymphocytosis, C2, C4, C4b, C3, C3a, Factor B, Bb, Facto
80 ting latently infected B cells, and a marked lymphocytosis caused by hyperexpansion of EBV-specific C
81 rcinoma, three (9%) cases of benign reactive lymphocytosis confirmed at open biopsy, and one (3%) cas
82 reduced CD4+ CD45RA+ T cells, and CD8+ CD57+ lymphocytosis, confirming the concept of a subgroup of p
86 s with these conditions have intraepithelial lymphocytosis, crypt hyperplasia, and severe intestinal
90 ubcutaneous infusion produced a much greater lymphocytosis, elevation in acute-phase reactants, and f
91 umor-bearing animals resulted in a transient lymphocytosis, followed by a clear reduction in tumor in
94 llus architecture, increased intraepithelial lymphocytosis, goblet cell depletion, Paneth cell deplet
95 a normal blood count and 2228 subjects with lymphocytosis (>4000 lymphocytes per cubic millimeter) f
97 the general population and in subjects with lymphocytosis have features in common with CLL cells.
99 only to subcutaneous and/or cutaneous sites, lymphocytosis immediately after treatment, and long-term
102 rheumatoid factor at onset of lung disease, lymphocytosis in bronchoalveolar lavage fluid (BALF), an
103 ported by positive precipitating antibodies, lymphocytosis in bronchoalveolar lavage fluid, and chara
105 ) inhibitor therapy induces peripheral blood lymphocytosis in chronic lymphocytic leukemia (CLL), whi
110 granulomatous lung lesions, peribronchiolar lymphocytosis, increased cell concentrations in lavage,
111 mmune activation was induced, as measured by lymphocytosis, increased peripheral-blood natural killer
112 cella antibodies in CSF; (3) the presence of lymphocytosis, increased protein, and decreased glucose
113 alatine petechiae, splenomegaly, or atypical lymphocytosis is associated with an increased likelihood
114 vine leukemia virus (BLV)-induced persistent lymphocytosis is characterized by a polyclonal expansion
116 ion characteristic of BLV-induced persistent lymphocytosis is IL-2 dependent and antigen dependent.
119 ymphoma cells associated with redistribution lymphocytosis, leading to more potent antitumour activit
120 ction, including oral transmission, atypical lymphocytosis, lymphadenopathy, activation of CD23(+) pe
122 logic entity usually characterized by marked lymphocytosis, massive splenomegaly, an aggressive cours
123 ria to distinguish between monoclonal B-cell lymphocytosis (MBL) and CLL could minimize patient distr
124 c lymphocytic leukemia (CLL) or monoclonal B-lymphocytosis (MBL) have impaired response to COVID-19 v
128 c leukemia (CLL)-phenotype monoclonal B-cell lymphocytosis (MBL) is a premalignant condition that is
134 cytic leukemia (CLL) -like monoclonal B-cell lymphocytosis (MBL) shares common immunophenotype and cy
135 ved in the transition from monoclonal B-cell lymphocytosis (MBL) to CLL and tested miR-15a/16-1 clust
136 kemia (CLL) is preceded by monoclonal B-cell lymphocytosis (MBL), a CLL precursor state with a preval
142 ated genes in CLL (5.3%) and in monoclonal B lymphocytosis (MBL, 7%), a B-cell expansion that can evo
144 t(14;18) translocation and monoclonal B-cell lymphocytosis, no clear link between the presence of abe
145 s presenting with lymphocytosis, progressive lymphocytosis occurred in 51 (28%), progressive CLL deve
150 D8+ T-lymphocyte ratio, and marked pulmonary lymphocytosis on histologic examination when compared wi
152 -associated viral loads without a marked CD8 lymphocytosis or NK cell disturbance like those seen in
153 ontrary, eosinophilia (OR, 1.6; P = 0.0002), lymphocytosis (OR, 1.84; P = 0.0002), increased erythroc
156 disease categories such as monoclonal B-cell lymphocytosis (peripheral blood clonal lymphocytosis tha
159 e mechanism of leukemogenesis and persistent lymphocytosis (PL; benign expansion of B lymphocytes) in
161 patients are preceded by a monoclonal B-cell lymphocytosis precursor state, patterns of immune defect
163 antly higher prevalence of monoclonal B cell lymphocytosis, premalignant condition poorly described i
171 hepatitis C infection, including sinusoidal lymphocytosis, steatosis, portal lymphoid aggregates/fol
172 btained from patients with monoclonal B-cell lymphocytosis, suggesting a role for LEF-1 early in CLL
173 sponse to HIV-1, termed diffuse infiltrative lymphocytosis syndrome (DILS), which resembles autoimmun
174 f spondyloarthritis and Diffuse Infiltrative Lymphocytosis Syndrome has decreased, whereas the muscul
175 V-infected persons with diffuse infiltrative lymphocytosis syndrome, a disease in which host immunoge
176 er manifestation of the diffuse infiltrative lymphocytosis syndrome, usually associated with a milder
179 ay marked lymphadenopathy, splenomegaly, and lymphocytosis, TDAG51-/- mice had no apparent defects in
181 -cell lymphocytosis (peripheral blood clonal lymphocytosis that does not meet other criteria for CLL)
182 e, many studies have attempted to define the lymphocytosis that occurs during acute EBV infection in
184 This illness is characterized by a striking lymphocytosis, the nature of which has been controversia
185 esponse and 10% with a partial response with lymphocytosis; the remaining 5% of patients had stable d
186 sponse and six (40%) a partial response with lymphocytosis; the remaining three (20%) patients had st
189 Cell mobilization studies revealed that the lymphocytosis was attributable to a combination of block
193 s with late-stage disease, termed persistent lymphocytosis, was significantly decreased compared to t
194 D4/CD8 ratio, increased blood CD8 count, and lymphocytosis were additional biomarkers highly correlat
195 t of 185 subjects with CLL-phenotype MBL and lymphocytosis were monitored for a median of 6.7 years (
196 morrhagic lesions, and cerebral spinal fluid lymphocytosis were significantly associated with HSV/VZV
197 etermined significance and monoclonal B-cell lymphocytosis, which are precursor states for hematologi
198 egories: chronic T-cell leukemia and NK-cell lymphocytosis, which are similarly indolent diseases cha
199 of lymphadenopathy accompanied by transient lymphocytosis, which is reversible upon temporary drug d
201 and clinical significance of a clonal B-cell lymphocytosis with an immunophenotype consistent with ma
203 ow cytometry showed that BIV causes a B-cell lymphocytosis with no consistent, significant changes in
204 sponse rate, including partial response with lymphocytosis, with acalabrutinib was 94%; responses wer
206 (KO) mice develop a progressive nonlethal B lymphocytosis, with expansion of B220(+) cells in the bo